Exogenous Norepinephrine Correlates with Macrophage Endoplasmic Reticulum Stress Response in Association with XBP-1

Yang, Chen; Zhou, Jianyun; Zhong, He-Jiang; Wang, Haiyan; Yan, Jun; Liu, Qing; Huang, Suna; Jiang, Jianxin

doi:10.1016/j.jss.2009.10.002

Cited by 12 publications

(10 citation statements)

References 40 publications

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“…Briefly, 100 μ L RPMs suspension (1.3 × 10 5 /well) was deposited in the insert and 600 μ L RPMI-1640 containing FMLP (Sigma-Aldrich) (0.1 mmol) was added into the lower compartment to induce chemotaxis for 2 h [25]. After the nonmigrated cells were removed from the polycarbonate membrane upper side, the migrated cells which were on the lower side were fixed and stained by crystal violet staining solution (Beyotime Institute of Biotechnology).…”

Section: Methodsmentioning

confidence: 99%

Altered Polarization, Morphology, and Impaired Innate Immunity Germane to Resident Peritoneal Macrophages in Mice with Long-Term Type 2 Diabetes

Liu

Zhang

et al. 2012

Journal of Biomedicine and Biotechnology

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Type 2 diabetes (T2D) is associated with perturbed innate immunity. Macrophages, bridging innate immunity and metabolic disturbances, play important roles in controlling immune homeostasis. However, the effect of long-term diabetic milieu (DM) on the functions and phenotypes of macrophages is still not clear. In this study, we used resident peritoneal macrophages (RPMs) from 5-month-old db/db mice to investigate the changes of macrophages. It was found that RPMs in db/db mice significantly reduced phagocytosis and adhesion capacity. After standardization with body weight, the number of F4/80+ RPMs markedly reduced in db/db mice, and, furthermore, the macrophages skewed to M2-polarizated macrophages. The results of morphology found that the RPMs shape of db/db mice was nearly round, but the RPMs shape of control mice was spindle-shaped and irregular. In this study, we found the cell numbers, morphology, and innate immunity functions of RPMs in 5-month-old type 2 diabetic mice (db/db mice) obtained by abdominal cavity lavage were significantly altered. Importantly, we also found the remarkably increased M2-RPMs in diabetic mice for the first time.

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Section: Methodsmentioning

confidence: 99%

Altered Polarization, Morphology, and Impaired Innate Immunity Germane to Resident Peritoneal Macrophages in Mice with Long-Term Type 2 Diabetes

Liu

Zhang

et al. 2012

Journal of Biomedicine and Biotechnology

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“…The ANS belongs to the neuromodulatory route secondary to the HPA axis in traumatic inflammation. The norepinephrine releasing from the sympathetic nervous ending could affect the immune system 81 . It was reported that a suppressive role for noradrenergic innervation on the hemorrhage-induced increase in lung TNF-α content in vivo 82 .…”

Section: The Dynamic Regularity Of Neuroendocrine Immune Network In Tmentioning

confidence: 99%

Altered Neuroendocrine Immune Responses, a Two-Sword Weapon against Traumatic Inflammation

Yang

Gao

et al. 2017

Int. J. Biol. Sci.

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During the occurrence and development of injury (trauma, hemorrhagic shock, ischemia and hypoxia), the neuroendocrine and immune system act as a prominent navigation leader and possess an inter-system crosstalk between the reciprocal information dissemination. The fundamental reason that neuroendocrinology and immunology could mix each other and permeate toward the field of traumatology is owing to their same biological languages or chemical information molecules (hormones, neurotransmitters, neuropeptides, cytokines and their corresponding receptors) shared by the neuroendocrine and immune systems. The immune system is not only modulated by the neuroendocrine system, but also can modulate the biological functions of the neuroendocrine system. The interactive linkage of these three systems precipitates the complicated space-time patterns for the courses of traumatic inflammation. Recently, compelling evidence indicates that the network linkage pattern that initiating agents of neuroendocrine responses, regulatory elements of immune cells and effecter targets for immune regulatory molecules arouse the resistance mechanism disorders, which supplies the beneficial enlightenment for the diagnosis and therapy of traumatic complications from the view of translational medicine. Here we review the alternative protective and detrimental roles as well as possible mechanisms of the neuroendocrine immune responses in traumatic inflammation.

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“…Peritoneal macrophages were collected from rats and purified [5, 6]. Macrophages (2 × 10 6 cells/well) were cultured in RPMI 1640 containing 10% fetal bovine serum (FBS) (Hyclone, USA) in a 24-well plate overnight at 37°C and 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Then, macrophages were stimulated with 10 ng/mL LPS ( Escherichia coli O26:B6) for another hour under the same conditions. Supernatant was collected, and the expressions of TNFα, IL-1 β , IL-6, and IL-10 were detected by an enzyme-linked immunosorbent assay (ELISA) kit (R&D Systems, USA; Boster Biotechnology, China) [5, 6]. Meanwhile, the adherent cell monolayer was washed with PBS, and 2 × 10 8 colony-forming units/mL of red-fluorescently labeled E. coli BI21 was added.…”

Section: Methodsmentioning

confidence: 99%

Epinephrine Enhances the Response of Macrophages under LPS Stimulation

Zhou

Yan

Liang

et al. 2014

BioMed Research International

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Trauma associated with infection may directly trigger a neuroendocrine reaction in vivo while the hormone epinephrine is known to mediate immune responses to inflammation after injury. However, the role of epinephrine during the earliest stage of trauma still remains unclear. We therefore explored the role of epinephrine on activated macrophages under LPS stimulation in vitro as well as the mechanisms underlying its effect. Dose- and time-dependent effects of epinephrine on macrophage immune function were assessed after LPS activation. We also employed CD14 siRNA interference to investigate whether CD14 played a role in the mechanism underlying the effect of epinephrine on LPS-induced macrophage responses. Our results showed that epinephrine pretreatment (10 ng/mL) significantly promoted immune responses from LPS stimulated macrophages, including phagocytic rate, phagocytic index, TNFα/IL-1β/IL-10 secretion, and CD14 expression (P < 0.05). Moreover, TNFα/IL-1β/IL-10 levels attained their peak value 1 hour after incubation with 10 ng/mL epinephrine (P < 0.05), and CD14 siRNA transfection dramatically decreased phagocytosis and cytokine secretion by LPS-activated macrophages (P < 0.05). We therefore conclude that 10 ng/mL epinephrine enhances immune responses from macrophages under LPS stimulation and that the underlying mechanism may relate to CD14 upregulation on the surface of macrophages.

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Exogenous Norepinephrine Correlates with Macrophage Endoplasmic Reticulum Stress Response in Association with XBP-1

Cited by 12 publications

References 40 publications

Altered Polarization, Morphology, and Impaired Innate Immunity Germane to Resident Peritoneal Macrophages in Mice with Long-Term Type 2 Diabetes

Altered Polarization, Morphology, and Impaired Innate Immunity Germane to Resident Peritoneal Macrophages in Mice with Long-Term Type 2 Diabetes

Altered Neuroendocrine Immune Responses, a Two-Sword Weapon against Traumatic Inflammation

Epinephrine Enhances the Response of Macrophages under LPS Stimulation

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